A positive correlation between IL-32 expression and infiltration of active NK cells was found in cutaneous melanoma.195 In a mouse model geared to understanding interactions between the immune system and the TME, the formyl peptide receptor (FPR) agonist WKYMVm promoted the migration of NK cells toward B16 melanoma cells and repressed tumor growth, whereas the FPR antagonist WRW (4) had the opposite effect.196. The gene discussed is FPR1; the disease is cutaneous melanoma.